Special relativity (SR) determines the properties of synchrotron radiation, but the corresponding mechanisms are frequently misunderstood. Time dilation is often invoked among the causes, whereas its role would violate the principles of SR. Here it is shown that the correct explanation of the synchrotron radiation properties is provided by a combination of the Doppler shift, not dependent on time dilation effects, contrary to a common belief, and of the Lorentz transformation into the particle reference frame of the electromagnetic field of the emission-inducing device, also with no contribution from time dilation. Concluding, the reader is reminded that much, if not all, of our argument has been available since the inception of SR, a research discipline of its own standing.

ABSTRACT In pathological left ventricular hypertrophy (LVH) with a normal intrinsic myocardial function, eccentric chamber remodelling (cardiac dilatation) can produce a right shift in systolic pressure-volume (P-V) relations (systolic chamber dysfunction). Whether comparable degrees of cardiac dilatation in physiological (exercise-induced eccentric left ventricular remodelling) and pathological LVH produce similar effects on chamber function has not been determined. Hence, the aim of my thesis was to determine the impact of cardiac dilatation on systolic chamber function in chronically exercised rats with comparable increases in cardiac diastolic volumes as those produced by two rat models of pathological dilatation. Methods: Two models of cardiac dilatation were used, namely: (1) a model of pathological cardiac hypertrophy and dilatation (induced by chronic β-adrenoreceptor agonist administration to either Sprague-Dawley or spontaneously hypertensive rats), and (2) a model of physiological cardiac hypertrophy and dilatation (induced in Sprague-Dawley rats by 4-5 months of voluntary running activity on exercise wheels). 33 Sprague-Dawley rats were placed on spontaneous running wheels for 4-5 months (Exer group) and 24 Sprague-Dawley sedentary control rats (Con group) were placed individually in normal rat cages. To induced pathological dilatation, the β-agonist, isoproterenol (ISO) was administered daily to Sprague-Dawley rats for 7 months (SD-ISO, n=10) and to spontaneously hypertensive rats (SHR) for 4-5 months (SHR+ISO, n=22). Saline was administered daily to controls (SD, n=10; SHR, n=21) and to normotensive Wistar Kyoto rats (WKY, n=17). In isolated, perfused heart preparations, left ventricular (LV) dilatation was determined from the diastolic pressure-volume (P-V) relation and the volume intercept of the diastolic P-V relation (LV V0). Systolic chamber function was assessed by comparing LV developed pressures at specific filling volumes. Intrinsic systolic myocardial function was determined from the slope of the LV systolic developed stress-strain relation (myocardial systolic elastance). Results: ISO adminstered to SD and to SHR rats produced cardiac dilatation [LV V0 (ml): SD 0.20±0.01, SD-ISO 0.27±0.02, p<0.005; SHR 0.21±0.01, SHR-ISO 0.30±0.01, p<0.001], systolic chamber dysfunction (decrease in left ventricular developed pressures at incremental filling volumes) but normal intrinsic systolic myocardial function. Habitual exercise resulted in a right shifted LV diastolic P-V relation and an increased LV V0 (Exer 0.22±0.01, Con 0.18±0.01, p<0.005). In exercised rats (Exer-dilated, n=10) with equivalent dilatation as SD-ISO and SHR-ISO (LV V0 within 95% CI of SD-ISO and SHR-ISO), despite comparable LV diastolic P-V relations and LV V0 values (0.28±0.01); both systolic chamber function and intrinsic systolic myocardial function were normal. Conclusions: These data provide evidence to indicate that as compared to pathological dilatation, a similar extent of exercise-induced dilatation does not produce the same adverse effects on systolic chamber function.

Under effective compression, impingement of opposing rough surfaces of a fracture can force the walls of the fracture apart during slip. Therefore, a fracture’s surface roughness exerts a primary control on the amount of dilation that can be sustained on a fracture since the opposing surfaces need to remain in contact. Previous work has attempted to characterize fracture surface roughness through topographic profiles and power spectral density analysis, but these metrics describing the geometry of a fracture’s surface are often non-unique when used independently. However, when combined these metrics are affective at characterizing fracture surface roughness, as well as the mechanisms affecting changes in roughness with increasing slip, and therefore changes in dilation. These mechanisms include the influence of primary grains and pores on initial fracture roughness, the effect of linkage on locally increasing roughness, and asperity destruction that limits the heights of asperities and forms gouge. This analysis reveals four essential stages of dilation during the lifecycle of a natural fracture, whereas previous slip-dilation models do not adequately address the evolution of fracture surface roughness: (1) initial slip companied by small dilation is mediated by roughness controlled by the primary grain and pore dimensions; (2) rapid dilation during and immediately following fracture growth by linkage of formerly isolated fractures; (3) wear of the fracture surface and gouge formation that minimizes dilation; and (4) between slip events cementation that modifies the mineral constituents in the fracture. By identifying these fundamental mechanisms that influence fracture surface roughness, this new conceptual model relating dilation to slip has specific applications to Enhanced Geothermal Systems (EGS), which attempt to produce long-lived dilation in natural fractures by inducing slip. / Geology

Balloon dilatation of the stenosed mitral valve, in an attempt to relieve symptoms, was developed to replace the surgical procedure of closed mitral valvotomy. This procedure, whereby a balloon tipped catheter is introduced from the femoral vein and directed across the mitral valve after an atrial septal puncture, was developed in 1982. The procedure was first performed at Groote Schuur Hospital in 1988. Two types of dilating balloon (Inoue and Bifoil types) have been used. The aim of this retrospective study was to analyze the results of balloon mitral valvuloplasty procedures performed from 1988 until November 1992. In addition a detailed analysis was made of all complications of the procedure. 118 patients (mean age 30.7 years) underwent 124 attempted procedures. 93 % of attempts were successfully completed and an optimal result was achieved in 76% of patients. Mitral valve area increased from 0.9cm² to 2.0cm². Equivalent results have been achieved with both balloon types. Death occurred in 1.6 % of patients. 2.4 % of patients had severe mitral regurgitation as a complication. 4% of procedures resulted in cardiac chamber perforation. The experience at Groote Schuur has been similar to other centres treating young patients with rheumatic mitral stenosis.

Research has shown that a frame for an n-dimensional real Hilbert space offers phase retrieval if and only if it has the complement property. There is a geometric characterization of general frames, the Han-Larson-Naimark Dilation Theorem, which gives us the necessary and sufficient conditions required to dilate a frame for an n-dimensional Hilbert space to a frame for a Hilbert space of higher dimension k. However, a frame having the complement property in an n-dimensional real Hilbert space does not ensure that its dilation will offer phase retrieval. In this thesis, we will explore and provide what necessary and sufficient conditions must be satisfied to dilate a phase retrieval frame for an n-dimensional real Hilbert space to a phase retrieval frame for a k-dimensional real Hilbert.

The endothelium is an integral mediator of vascular homeostasis and a dysfunctional endothelium is now recognized as an early marker of atherosclerosis. Importantly, the non-invasive measurement of endothelial function by flow-mediated dilation (FMD) predicts future cardiovascular events. However, the appropriate method of its assessment and the mechanisms that govern FMD are still poorly understood. We investigated alternative parameters and methods of FMD measurement in healthy volunteers and cardiovascular disease patients. We found time to peak FMD to be highly variable both within and between individuals. Accordingly, continuous arterial diameter measurement post-cuff release was more sensitive in discriminating between health and disease compared to the measurement of diameter at 60’’ post-cuff release. Reperfusion to an ischemic tissue can paradoxically contribute to endothelial dysfunction development and further tissue damage, in a phenomenon known as ischemia and reperfusion (IR) injury. Previous exposure to sublethal ischemia (ischemic preconditioning (IPC)) can reduce sensitivity to IR injury and pharmacologic agents have since been shown to mimic this response. Using the FMD technique, we investigated various preconditioning strategies to prevent IR-induced endothelial dysfunction in the forearm vasculature of healthy volunteers. The sodium-hydrogen exchanger inhibitor amiloride and the angiotensin-converting enzyme inhibitor captopril were found not to provide endothelial protection from IR. In contrast, potent protection from IR-induced endothelial dysfunction was observed during the high-estrogen, late follicular phase of the menstrual cycle in pre-menopausal women. Finally, daily episodes of IPC were found to provide endothelial protection equipotent to an acute episode of IPC. The findings from the FMD methodological study highlight the importance of continuous arterial diameter measurement post-cuff deflation, and provide mechanistic insight that may contribute to measurement standardization and normalization. The results of the preconditioning studies improve our understanding of potential approaches to mitigate the detrimental effects of IR on the endothelium in humans.

The endothelium is an integral mediator of vascular homeostasis and a dysfunctional endothelium is now recognized as an early marker of atherosclerosis. Importantly, the non-invasive measurement of endothelial function by flow-mediated dilation (FMD) predicts future cardiovascular events. However, the appropriate method of its assessment and the mechanisms that govern FMD are still poorly understood. We investigated alternative parameters and methods of FMD measurement in healthy volunteers and cardiovascular disease patients. We found time to peak FMD to be highly variable both within and between individuals. Accordingly, continuous arterial diameter measurement post-cuff release was more sensitive in discriminating between health and disease compared to the measurement of diameter at 60’’ post-cuff release. Reperfusion to an ischemic tissue can paradoxically contribute to endothelial dysfunction development and further tissue damage, in a phenomenon known as ischemia and reperfusion (IR) injury. Previous exposure to sublethal ischemia (ischemic preconditioning (IPC)) can reduce sensitivity to IR injury and pharmacologic agents have since been shown to mimic this response. Using the FMD technique, we investigated various preconditioning strategies to prevent IR-induced endothelial dysfunction in the forearm vasculature of healthy volunteers. The sodium-hydrogen exchanger inhibitor amiloride and the angiotensin-converting enzyme inhibitor captopril were found not to provide endothelial protection from IR. In contrast, potent protection from IR-induced endothelial dysfunction was observed during the high-estrogen, late follicular phase of the menstrual cycle in pre-menopausal women. Finally, daily episodes of IPC were found to provide endothelial protection equipotent to an acute episode of IPC. The findings from the FMD methodological study highlight the importance of continuous arterial diameter measurement post-cuff deflation, and provide mechanistic insight that may contribute to measurement standardization and normalization. The results of the preconditioning studies improve our understanding of potential approaches to mitigate the detrimental effects of IR on the endothelium in humans.

Flow-mediated dilation (FMD) refers to the relaxation of vascular smooth muscle and the subsequent dilation of the vessel in response to increases in shear stress on the endothelial lining accompanying increases in blood flow. The phenomenon has been shown to be endothelium dependent and as such is used clinically and experimentally as an index of endothelial health. FMD can be assessed by imaging a conduit artery with ultrasound during a period of reactive hyperaemia, typically following a period of prior blood flow occlusion achieved by the inflation of a pneumatic cuff around the limb distal to the imaging site. Previous studies have shown that the health of the endothelium is predictive of the health of the cardiovascular system as a whole. This thesis set out to scrutinize the FMD test as a marker for endothelial health by testing the following five hypotheses: 1. A short burst of high shear is not adequate to elicit the FMD response. 2. Brachial artery dilation following 15 minutes of occlusion is a clearer indicator of endothelium dependent FMD than 5 minutes of occlusion with exercise. 3. Oscillating the post occlusion shear stress will decrease FMD compared to unidirectional shear). 4. Heavy dynamic hand grip exercise 6 minutes before an occlusion-only FMD protocol will result in an enhanced FMD response. 5. Long term bed-rest inactivity will attenuate the FMD response and an exercise program will preserve endothelial function. The experiments documented in Chapter 2 found that a 20-s shear stress stimulus following 15 min of forearm circulatory occlusion was not adequate to induce an FMD response compared to longer durations of shear and there was a progressive reduction in FMD when the magnitude of the initial peak shear was reduced by limiting the duration of prior occlusion. Also, the FMD response was correlated with the total shear to time of peak diameter for all shear durations and peaks that were studied while the same was not true of peak shear. In Chapter 3 it was revealed that an uncoupling of the shear-to-dilation ratio occurred when dynamic exercise was added to the FMD test as both 15 min of occlusion (15OC) and 5 min of occlusion with 1 min of exercise (1EXin5OC) yielded similar FMD responses, even though the shear stimulus was increased with the addition of exercise. Increased plasma nitrite during hyperaemia was observed only in the 15OC protocol, suggesting that the exercise in the 1EXin5OC protocol initiates dilatory mechanisms that are not as heavily reliant on the shear sensitive nitric oxide pathway . In Chapter 4 it was shown that 5 min of intense dynamic hand grip exercise (5EX) produced a greater dilation than either continuous (15OC) or intermittent (IO) shear following 15OC. Total shear to the time of peak diameter (AUCshear) and peak shear were both correlated to %dilation following 15OC; however this relationship was lost during 5EX and IO. The results of this study echoed the suggestion in Chapter 3 that there was an uncoupling of the intensity of the shear stimulus and the magnitude of vasodilatation when exercise was introduced, and adds that it may be in part due to the oscillatory nature of the shear profile during exercise. The acute effects of local exercise on the FMD response following 15OC were examined in Chapter 5. FMD in the brachial artery was blunted following dynamic hand grip exercise, even though the shear stimulus was greater during PostEX. Nitrite was significantly elevated in CON at 15s while PostEX nitrite was significantly elevated at 30s post cuff release but not different from CON at 15s. The results of this study suggested that prior exercise had a negative effect on FMD which may be related to exercise blunting post occlusion endothelial N ̇O production. Chapter 6 examined the effect of 56 days of head-down tilt bed rest (HDBR) and an exercise countermeasure on conduit artery FMD following release of distal limb ischemia and NMD following sublingual administration of 0.3 mg of nitroglycerin. HDBR without EX decreased the resting diameter of the popliteal artery while EX increased the diameter. HDBR had no effect on the resting diameter of the brachial artery. FMD was elevated in all groups for the brachial but only in the non-exercisers for the popliteal. When change in resting diameter was taken into account the preserved FMD in EX was removed. NMD was not altered by HDBR in any group. There was enhanced endothelial function relative to intrinsic dilatory capacity in both the brachial and popliteal arteries post HDBR. The results from Chapter 2 support hypothesis 1, showing that a 20 second burst of high shear stimulus was not adequate to elicit the FMD response during reactive hyperaemia. It is not clear whether hypothesis 2 was supported or not given that the results from Chapter 3 showed on the one hand that the %FMD did not change with the addition of exercise in the occlusion but on the other hand the shear to dilation ratio was altered. The finding, in Chapter 4, that FMD was not reduced when the hyperaemia was intermittent does not support hypothesis 3. In opposition to hypothesis 4, Chapter 5 showed that %FMD was reduced following bouts of heavy hand grip exercise; however the absolute magnitude of vessel diameter was similar in both post exercise and control tests. Finally, hypothesis 5 was also contradicted, with Chapter 6 showing that long term bed-rest enhanced rather than attenuated the FMD response in both arm and leg arteries, while an exercise countermeasure preserved pre-bed-rest FMD in the legs only. In addition to the specific hypotheses tested, there was evidence that acute exercise evoked dilatory mechanisms in the conduit arteries that were not shear/endothelium dependent given that the shear to dilation relationship was uncoupled during, following, and in occlusion protocols that include exercise. The precise mechanisms by which this is achieved are still unknown, but it may be partially due to the oscillatory nature of the elevated blood flow during exercise. I conclude that inference of cardiovascular health from endothelial function by the evaluation of %FMD should be approached with caution, especially in the event that physical activity is involved.

Flow-mediated dilation (FMD) refers to the relaxation of vascular smooth muscle and the subsequent dilation of the vessel in response to increases in shear stress on the endothelial lining accompanying increases in blood flow. The phenomenon has been shown to be endothelium dependent and as such is used clinically and experimentally as an index of endothelial health. FMD can be assessed by imaging a conduit artery with ultrasound during a period of reactive hyperaemia, typically following a period of prior blood flow occlusion achieved by the inflation of a pneumatic cuff around the limb distal to the imaging site. Previous studies have shown that the health of the endothelium is predictive of the health of the cardiovascular system as a whole. This thesis set out to scrutinize the FMD test as a marker for endothelial health by testing the following five hypotheses: 1. A short burst of high shear is not adequate to elicit the FMD response. 2. Brachial artery dilation following 15 minutes of occlusion is a clearer indicator of endothelium dependent FMD than 5 minutes of occlusion with exercise. 3. Oscillating the post occlusion shear stress will decrease FMD compared to unidirectional shear). 4. Heavy dynamic hand grip exercise 6 minutes before an occlusion-only FMD protocol will result in an enhanced FMD response. 5. Long term bed-rest inactivity will attenuate the FMD response and an exercise program will preserve endothelial function. The experiments documented in Chapter 2 found that a 20-s shear stress stimulus following 15 min of forearm circulatory occlusion was not adequate to induce an FMD response compared to longer durations of shear and there was a progressive reduction in FMD when the magnitude of the initial peak shear was reduced by limiting the duration of prior occlusion. Also, the FMD response was correlated with the total shear to time of peak diameter for all shear durations and peaks that were studied while the same was not true of peak shear. In Chapter 3 it was revealed that an uncoupling of the shear-to-dilation ratio occurred when dynamic exercise was added to the FMD test as both 15 min of occlusion (15OC) and 5 min of occlusion with 1 min of exercise (1EXin5OC) yielded similar FMD responses, even though the shear stimulus was increased with the addition of exercise. Increased plasma nitrite during hyperaemia was observed only in the 15OC protocol, suggesting that the exercise in the 1EXin5OC protocol initiates dilatory mechanisms that are not as heavily reliant on the shear sensitive nitric oxide pathway . In Chapter 4 it was shown that 5 min of intense dynamic hand grip exercise (5EX) produced a greater dilation than either continuous (15OC) or intermittent (IO) shear following 15OC. Total shear to the time of peak diameter (AUCshear) and peak shear were both correlated to %dilation following 15OC; however this relationship was lost during 5EX and IO. The results of this study echoed the suggestion in Chapter 3 that there was an uncoupling of the intensity of the shear stimulus and the magnitude of vasodilatation when exercise was introduced, and adds that it may be in part due to the oscillatory nature of the shear profile during exercise. The acute effects of local exercise on the FMD response following 15OC were examined in Chapter 5. FMD in the brachial artery was blunted following dynamic hand grip exercise, even though the shear stimulus was greater during PostEX. Nitrite was significantly elevated in CON at 15s while PostEX nitrite was significantly elevated at 30s post cuff release but not different from CON at 15s. The results of this study suggested that prior exercise had a negative effect on FMD which may be related to exercise blunting post occlusion endothelial N ̇O production. Chapter 6 examined the effect of 56 days of head-down tilt bed rest (HDBR) and an exercise countermeasure on conduit artery FMD following release of distal limb ischemia and NMD following sublingual administration of 0.3 mg of nitroglycerin. HDBR without EX decreased the resting diameter of the popliteal artery while EX increased the diameter. HDBR had no effect on the resting diameter of the brachial artery. FMD was elevated in all groups for the brachial but only in the non-exercisers for the popliteal. When change in resting diameter was taken into account the preserved FMD in EX was removed. NMD was not altered by HDBR in any group. There was enhanced endothelial function relative to intrinsic dilatory capacity in both the brachial and popliteal arteries post HDBR. The results from Chapter 2 support hypothesis 1, showing that a 20 second burst of high shear stimulus was not adequate to elicit the FMD response during reactive hyperaemia. It is not clear whether hypothesis 2 was supported or not given that the results from Chapter 3 showed on the one hand that the %FMD did not change with the addition of exercise in the occlusion but on the other hand the shear to dilation ratio was altered. The finding, in Chapter 4, that FMD was not reduced when the hyperaemia was intermittent does not support hypothesis 3. In opposition to hypothesis 4, Chapter 5 showed that %FMD was reduced following bouts of heavy hand grip exercise; however the absolute magnitude of vessel diameter was similar in both post exercise and control tests. Finally, hypothesis 5 was also contradicted, with Chapter 6 showing that long term bed-rest enhanced rather than attenuated the FMD response in both arm and leg arteries, while an exercise countermeasure preserved pre-bed-rest FMD in the legs only. In addition to the specific hypotheses tested, there was evidence that acute exercise evoked dilatory mechanisms in the conduit arteries that were not shear/endothelium dependent given that the shear to dilation relationship was uncoupled during, following, and in occlusion protocols that include exercise. The precise mechanisms by which this is achieved are still unknown, but it may be partially due to the oscillatory nature of the elevated blood flow during exercise. I conclude that inference of cardiovascular health from endothelial function by the evaluation of %FMD should be approached with caution, especially in the event that physical activity is involved.

This study evaluated the soil properties of clean sand, a silty sand, and a road base that are extensively used as a backfill for full-scale testing at Riverside Campus at Texas A&M University. The three soils were collected at the Riverside Campus and the testing schedule included grain size analysis, hydrometer test, specific gravity, maximum dry density, Atterberg limit, stiffness, direct shear test, triaxial test, and a simple procedure to estimate the maximum and minimum void ratio of the clean sand. Relation between strength/deformation, vertical displacement/shear displacement, and physical properties were evaluated to estimate the frictional resistance and angle of dilation of the clean sand and the silty sand. Numerical simulations of the Direct Shear Test (DST) were conducted on the clean sand using Finite Element Model in the computer program LS-DYNA. The simulations were intended to reproduce the Direct Shear Test (DST) to estimate the frictional resistance and dilatancy effects of the clean sand under different compressive stresses. Field tests were also conducted on the clean sand and the road base. These tests included the in-situ density determination, in-situ water content, and the soil modulus using the Briaud Compaction Device (BCD).